Echidnas blow snot bubbles to keep their noses cool

January 23, 2023 • 11:15 am

You’ve heard about about platypuses, the monotreme egg-laying mammal that lays eggs, a primitive condition inherited from the ancestor of all modern mammals (and their earlier reptilian ancestors). But perhaps you also know of the “echidnas“, or “spiny anteaters” (not very related to regular anteaters), also in the order Monotremata and the only other egg-laying mammal. (These are not marsupials; they diverged from the placental/marsupial mammal group, called therians, between 250 and 160 million years ago.)

The living monotremes comprise four species of echidna and only one species of platypus (Ornithorhynchus anatinus), and these two groups diverged from each other between 57 and 21 million years ago. Further, the monotremes diverged from the “regular” (therian) mammals between 218 and 187 million years ago.

The article at hand is about one of the four echidna species, the short beaked-echidna (Tachyglossus aculeatus). Here’s what it looks like:

Click on the article below to read about how echidnas keep cool in the hot climate of Australia (the pdf is here, the full reference is at at bottom, and there’s a popular article here.  But the article below, from Biology Letters published by Britain’s Royal Society, is short and easy to read:

So the issue is this: earlier studies had demonstrated that this species had a low thermal tolerance, with a lethal core body temperature of 38ºC (100.4º F) and a lethal air temperature of just 35ºC (95º F). (From now on I’ll just give the Celsius temperatures, as you should get familiar with the conversion.) Yet the echidna is found in Australian habitats where the air temperature is higher than this, so they must have a way to cool off. The paper reports thermal-imaging studies of wild echidnas to see how they do this.

Clearly, the echidna must have some way to lower the temperature it encounters in the wild, which the authors call a “thermal window” or “regions of the animal’s body surface that vary heat exchange with the environment being ‘opened’ or ‘closed’ by changes in exposure and/or blood flow.” (Below are some cool examples of how other species do this.)

The authors measured the echidnas’ body temperature by thermal imaging, and estimated the ambient temperature as the average of the air temperature and tje ground temperature. They also measured a “wet bulb” temperature, which is the temperature measured by a wetted thermometer bulb. Wet-bulb temperature is cooler than the air temperature because the evaporation of the water from the bulb cools it off.

They found two ways that echidnas cool themselves off at higher temperatures. The temperature comparisons of echidna body parts with environmental temperature was measured by plotting, over a variety of echidnas observed at different temperatures, the wet bulb temperature (x axis) versus the surface temperature of the animal (y axis).  That’s shown below, but first one observation.

The first way of cooing the authors found was seeing the animals press their relatively furless (and spineless) inner leg an belly surfaces against the cool soil.  This is similar to what kangaroos do; see below. The spines also help keep the sun off their bodies, and there is a subcutaneous fat layer, into which the spines are embedded, that also provides insulation.

The second way of cooling is the swell finding given in the headline. You can see it below in the lower right section of the following graph. It shows body temperatures versus wet bulb temperature for various parts of the echidnas’ bodies (remember, this is done by thermal imaging). The body areas measured are shown in green, and the body temperatures measured at varying wet-bulb temperatures for each body area, are shown as dots, one for each echidna part measured. Measurements were done on 124 echidnas (some may have been duplicates, as they couldn’t identify individuals) at the Dryanra Woodland and Boyagin Nature Reserve in the West Australian wheatbelt, 170 k southwest of Perth, in western Australia:

 

(From paper): Figure 1. Surface temperature of various body regions plotted against wet bulb globe temperature (WBGT) for 124 active short-beaked echidnas (Tachyglossus aculeatus) filmed with an infrared camera in the West Australian wheatbelt. The solid line represents a slope = 1 for WBGT, the dashed line the observed slope for the relationship; asterisks indicate that the slope is significantly different from 1. The inset thermal image shows the body region represented by each panel, outlined with a green polygon.

What you see is that the surface temperature (the height of the dots) is, for six regions of the body, higher than the wet-bulb temperature, which means there’s no evaporative cooling of those warm body surfaces. But look at the “beak tip” at lower right. At all the wetbulb temperatures, the beak tip temperature is the same as the wet-bulb temperature. That means that somehow there is extra cooling going on at the tip of the snout.

How do they do this? They blow snot bubbles out their nose, which, when they burst, keep the nose moist, thus cooling the echidna. In effect, the the beak is a “snot bulb.” Or, to quote the authors:

We identify the beak tip of short-beaked echidnas as a unique type of evaporative window. The beak tip, containing a large dorsal blood sinus, is kept moist to facilitate electroreception. An additional role of this moist surface is evaporative cooling of the underlying blood within the sinus; with a slope equivalent to 1 and minimal intercept, the beak tip functions as a wet bulb globe thermometer. At high Ta [air temperature] echidnas blow mucus bubbles, adding moisture to the beak tip . This unique nasal evaporative window is of particular value for echidnas (which do not pant, lick or sweat) especially under conditions where environmental temperature exceeds Tb [core body temperature] and evaporation is the only avenue available for heat loss.

Here’s a video from Science News about the cooling.  Note that here the lightest areas are the hottest and the darkest are the coolest. Check out the snout tip, circled at 5 seconds in. It’s very dark!

Upshot: Echnidnas have evolved to cool themselves off by blowing snot bubbles when it’s hot. The bubbles’ bursting keeps the animal cool, especially because the snout is well equipped with lots of blood vessels that radiate the heat.

Here’s the authors’ description about how other species use evaporative cooling, including the fact that kangaroos lick their forearms to cool off when it’s hot:

. . . there have been few descriptions for endotherms of specialized evaporative windows where endogenous water is behaviourally applied to areas with specialized vasculature. The classic examples of evaporative windows are for storks and turkey vultures, which urinate on their legs that contain extensive subcutaneous vascularization, facilitating EHL. Seals on rocks similarly urinate to wet their ventral surface and vascularized flippers to enhance EHL, while the licking of vascularized forearms by macropods is the best-known mammalian example.

Storks and seals piss on themselves to cool off! I bet you didn’t know that.

Here’s an Attenborough video of red kangaroos (Osphranter rufus) cooling themselves by licking their highly vascularized forearms (you can skip to 2:05 to see it, as well as thermal images showing the cooling). They also stay in the shade and dig down into the cooler soil beneath the surface and lie down on the cool soil.

 

Now we can add to these examples of evaporative cooling the snot bubbles of echidnas.

h/t Greg Mayer

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Cooper C. E. and Withers PC. 2023. Postural, pilo-erective and evaporative thermal windows of the short-beaked echidna (Tachyglossus aculeatus).Biol. Lett.19: 20220495

Flannery, T.F., T.H. Rich, P. Vickers-Rich, T. Ziegler, E.G. Veatch, and K.M. Helge. 2022. A review of monotreme (Monotremata) evolution. Alcheringa 46(1): 3-20.

 

The remarkable physiology of hibernating bears

October 11, 2022 • 10:45 am

Have you been voting in Fat Bear Week? If not, today is the final day: the run-off between two heavyweights that will determine the Fattest Bear.

You probably realize that the bears get so fat in the fall because they are about to go into five months of hibernation, and need to stock up on food to sustain their metabolism as they go into winter. The Washington Post article shown below describes the remarkable phenomenon of hibernation, the potential bodily problems it poses, and new biochemical discoveries that help the bears obviate these issues and could also help immobile humans with the issue of atrophied muscles. Click to read:

Quotes from the article are indented:

But for many scientists, the true fascination of Fat Bear Week involves what happens next, when the now beachball-shaped bruins, carrying about 40 percent body fat, lumber into their dens and start hibernating. During hibernation, they remain healthy under conditions that would weaken and sicken mere humans. The bears emerge months later, lean, strong and barely affected by their months of starvation and inactivity.

Until recently, researchers could not explain how. But several fascinating new molecular studies suggest hibernation remodels bear metabolisms and gene activity in unique and dramatic ways that could have relevance for people. The fat bears can advance our understanding of diabetes, muscle atrophy, inactivity and the ingenuity of evolution.

Superficially, hibernating bears seem passive and inert. For five months or more, they do not eat, drink, urinate, defecate or move, except occasionally to turn over or shiver. Their metabolisms drop by about 75 percent. Hearts beat and lungs inflate only a few times a minute. Kidneys shut down. The bears grow profoundly insulin resistant.

If this were us, we would shed much of our muscle mass because of inactivity and probably develop diabetes, heart disease, kidney failure, frailty and other ills.

But the bears maintain their muscle and rapidly reestablish normal, healthy insulin sensitivity and organ function after hibernation.

Insulin functions to allow cells to absorb glucose from the blood to use as energy, or to convert some glucose to fat. It also helps break down fats and proteins. Normally, the onset of insulin resistance would, as the article implies, lead to diabetes and its attendant problems, but the bears are somehow able to tolerate that—as well as the muscle atrophy attendant on not moving for five months. (Muscle atrophy is a problem for people who are either paralyzed or bedridden for long periods of time.)

How do the bears do this? That’s the point of the article, which links to three scientific articles (one given below) explaining how the bears survive hibernation.

The information on fat usage came from blood samples drawn from hibernating and non-hibernating bears at Washington State University (WSU), bears trained to allow a blood draw without being anesthetized. (I guess the WSU bears also go into hibernation.)

It turns out that there is differential activation of genes in the bears during hibernation that protect them from deleterious effects of hibernation. Here are two papers cited:

By comparing the samples, [reserachers] concluded hibernation is biologically uncanny but hardly quiet. In a 2019 study, the WSU scientists and others found more than 10,000 genes in bears that work differently during hibernation vs. in autumn or spring. Many involve insulin activity and energy expenditure and most occur in the animals’ fat, which becomes quite insulin resistant during hibernation and robustly insulin sensitive immediately afterward.

Digging deeper into that process for a new study, published in September in iScience, they bathed fat cells drawn from hibernating and active bears with blood serum taken during the opposing time and watched the fat switch seasons. Fat from hibernating bears became insulin sensitive and genetically similar to fat from the active season and vice versa.

In other words, something in the blood serum of non-hibernating bears restored the insulin sensitivity of hibernating bears, and vice versa. This shows that it is something in the serum, and not in the fat, that changes during hibernation. The article continues:

Perhaps most compelling, they also identified and cross-matched hundreds of proteins in the animals’ blood and found eight that differed substantially in abundance from one season to the next. These eight proteins seemed to be driving most of the genetic and metabolic changes in the fat.

Of course correlation is not causation, and I doubt that 10,000 genes are involved in actually producing hibernation or mitigating its effects. (After all, humans have only about 25,000 protein-coding genes—more if you include as “genes” bits of DNA that do something but don’t produce proteins—and bears can’t differ that much from us. There may be changes in that many genes, but many of these may simply be side effects of natural selection changes the expression of many fewer genes.

But it’s clear that genes involved in insulin usage and sensitivity work differently in hibernating versus nonhibernating bears. What are the cues that turn these genes on and off? I doubt that we know, and the paper doesn’t say, but a good guess is that this has to do with environmental factors indicating the impending arrival of spring or fall: cues based on day length or temperature.

But what about the bears’ muscles? Why don’t they atrophy? Again, it’s due (as it must be) to differential activation of genes. And again, the gene products responsible seem to be circulated in the blood serum.

The paper below from PLoS ONE (click on screenshot to read; pdf here and reference at bottom), implicates both the blood serum and the genes involved in maintaining muscle.

The Japanese researchers bathed cultured human skeletal muscle cells in serum from either hibernating or non-hibernating black bears. What they found was significantly less degradation of protein when hibernating-bear serum was used. This appeared to be based on a gene-induced decrease in levels of two proteins and an increase in the level of another, which act in concert to preserve protein levels in the cultured cells. (The protein made in reduced amount breaks down muscle while the others promote and sustain muscle growth.) Altogether, changes in gene action appears to keep the bears’ muscles fairly intact as they go through hibernation.

Now these are cultured human cells, not bear cells, and the experiment was done in vitro rather than in vivo, but it gives a very promising lead to how bears keep their muscles strong during hibernation.

The Post article also lays out the potential uses of this information in human health.

Fat.

Potentially, these same eight proteins, which also appear in human blood, might at some point be harnessed pharmaceutically to improve insulin sensitivity or treat diabetes and other metabolic disorders in people, Kelley said. But that possibility lies far in the future and requires vastly more research with bears and us (although perhaps not in close proximity).

Muscle.

The ultimate aim of this research, [author] Miyazaki said, is to isolate and refine all of the substances and processes in hibernating bears’ blood and elsewhere in their bodies that protect them from muscle wasting, with the hope that these same elements might treat atrophy from bed rest or aging in people.

“There is probably no better way to maintain a healthy lifestyle than through physical exercise,” he said, but for people who cannot be active, for whatever reason, the internal operations of slumbering bears might someday provide respite from frailty.

It’s important to remember that these remarkable changes are certainly due to evolution via natural selection, as it’s hard to imagine a random process like genetic drift causing evolutionary changes that are certainly adaptive.

As Ernst Mayr emphasized, many important evolutionary changes in animals begin with a change in behavior. Perhaps bears in cold areas survived better if they underwent a period of low activity during winter when food is scarce (this behavioral change could reflect genetic variation), and then those quiescent bears who also had mutations affecting fat and muscle metabolism would be those most likely to survive hibernation, leaving their genes to future bear generations.

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Miyazaki M, Shimozuru M, Tsubota T. (2022) Supplementing cultured human myotubes with hibernating bear serum results in increased protein content by modulating Akt/FOXO3a signaling. PLoS ONE 17(1): e0263085. https://doi.org/10.1371/journal.pone.0263085

It’s Nobel Prize Week! Physiology/Medicine Prize awarded to pair for work on bodily temperature and touch sensors. Plus, our annual Guess-the-Laureate Contest.

October 4, 2021 • 8:45 am

Starting today and extending for a week, we’ll have a Nobel Prize awarded every weekday. The Physiology or Medicine Prize was announced this morning in Stockholm, and so two investigators will have been woken up early but will be very happy. Here they are with some info from the Howard Hughes Medical Institute (I’ve added links):

David Julius [left below], a professor at the University of California, San Francisco and a Howard Hughes Medical Institute (HHMI) Trustee, and Ardem Patapoutian [right], an HHMI Investigator at Scripps Research have received the award for their work identifying receptors on sensory neurons that give us the ability to monitor temperature, pain, touch, and movement of our body.

The prize was announced here and the explanation of what Julius and Patapoutian found is here or at the HHMI site.  Trigger warning: Hot peppers are involved! Here’s the official announcement (32 minutes), which gives the names and explains the discoveries as well with the explanation beginning at 2:23.

A tweet sent mr by Matthew:

Because the biology prize was announced already, it can’t be part of our annual contest to “Guess the Laureates”. Since nobody ever wins that one, I’m making it easier this year.

Look at the announcements below, and then guess the names of ONLY THREE LAUREATES, one from each of three of the five categories of your choice: physics, chemistry, literature, peace, or the economics prize. If there you have multiple guesses in a category, you can guess only one recipient. 

Remember: just give me three names and the area in which each is supposed to win. 

If you guess a name after the prize is awarded, your entry doesn’t count. So if you’re guessing in physics, your deadline is this evening, and so on.

If there is more than one winning entry (all three guesses correct), we will have a raffle for the winner. The Coyne Prize is, also as usual, an autographed copy of one of my two trade books (WEIT or Faith Versus Fact), with a picture drawn in (by me) of an animal of your choice.  I suggest that you enter (in the comments below) by the end of today.

***************

Here’s the schedule of announcements from the organization itself:

AWARDED: PHYSIOLOGY OR MEDICINE – Monday 4 October, 11:30 CEST at the earliest
The Nobel Assembly at Karolinska Institutet, Wallenbergsalen, Nobel Forum, Nobels väg 1, Solna
http://www.nobelprizemedicine.org
nobelforum@nobelprizemedicine.org

PHYSICS – Tuesday 5 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences (Kungl. Vetenskapsakademien, KVA), Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

CHEMISTRY – Wednesday 6 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences, Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

LITERATURE – Thursday 7 October, 13:00 CEST at the earliest
The Swedish Academy (Svenska Akademien), Börssalen, Källargränd 4, Stockholm
http://www.svenskaakademien.se/en
louise.hedberg@svenskaakademien.se

PEACE – Friday 8 October, 11:00 CEST
The Norwegian Nobel Committee, The Norwegian Nobel Institute (Norska Nobelinstitutet), Store Sal, Henrik Ibsens gate 51, Oslo
https://www.nobelpeaceprize.org
postmaster@nobel.no

THE SVERIGES RIKSBANK PRIZE IN ECONOMIC SCIENCES IN MEMORY OF ALFRED NOBEL – Monday 11 October, 11:45 CEST at the earliest
The Royal Swedish Academy of Sciences, Sessionssalen, Lilla Frescativägen 4A, Stockholm
www.kva.se/pressroom
eva.nevelius@kva.se

Are sponges the closest relatives of the rest of the animals?

March 21, 2021 • 9:30 am

A new paper in Nature Communications highlights an ongoing controversy in the evolution of animals: what are the closest relatives of living multicellular animals?

First, though, we need to refresh ourselves on what “animals” are. Merriam-Webster defines them adequately:

Any of a kingdom (Animalia) of living things including many-celled organisms and often many of the single-celled ones(such as protozoans) that typically differ from plants in having cells without cellulose walls, in lacking chlorophyll and the capacity for photosynthesis, in requiring more complex food materials (such as proteins), in being organized to a greater degree of complexity, and in having the capacity for spontaneous movement and rapid motor responses to stimulation.

We’re leaving out the single-celled “animals” here (under “outgroups” in the figure below) and concentrating on multicellular animals.

The multicellular animals include (as the phylogenies show below), Ctenophores, or comb jellies, Porifera (sponges), Placozoans (free living but small multicellular organisms), Cnidaria (corals, jellyfish, sea anemones and their relatives), and Bilateria (everything else; all animals with a head and tail end, as well as a belly and a back at some stage of their life, including echinoderms which have these features as larvae).  Over the years, a combination of developmental, morphological, and molecular analysis has given rise to the two conflicting family trees shown below.

Both trees are the same except for a dispute about the “animal outgroup” (the “breakaway group” or “sister group”), the closest living relative to the vast bulk of the animals, and the first group to branch off from the rest. One school, shown on the left, adheres to the ctenophores, or comb jellies, as this sister group. The other, shown on the right, maintains that sponges occupy this position, and ctenophores branched off later.

 

Here’s an example of a ctenophore (photos from Wikipedia):

And a bunch of sponges:

Now the case for sponges as the sister group is based on the observation that ctenophores share unique features with the other animals, including elements of nervous systems, and (except for Placozoans) muscles and a tubelike digestive system (“gut”). But sponges have none of these. Moreover, sponges are made up of collared cells, or choanocytes, which are similar to “choanoflagellates“, singled-celled protozoans thought to be the closest relative to all the animals from sponges on down. This similarity implies that the common ancestor of multicellular animals might have been something spongelike, supporting the second phylogeny above. That implies that sponges changed relatively little after multicellular animals evolved, while everything else changed a lot more.

But some molecular phylogenies have suggested that the more complex ctenophores might be the outgroup instead of sponges.  This is a bit more problematic to both me and Matthew (see his BBC broadcast below), for if sponges are really more closely related to other animals than are ctenophores, why do ctenophores have muscles, nerves, and an in—>out digestive system like most other animals, but sponges lack these things? To hold that ctenophores are the sister group instead of sponges requires that you posit one of two possibilities:

A.) The common ancestor of all animals had nervous systems and muscles and a gut, which persist in all groups but the sponges, and the sponges lost these features. That seems unlikely, but it’s possible.

or

B.) The common ancestor of all animals lacked these features, but they evolved independently in the choanoflagellates and all other animals save sponges. This seems even more unlikely since it requires the independent evolution of three complex traits in two separate groups (ctenophores and [other animals minus sponges]).

This principle of “parsimony” alone suggests that sponges are the sister group, didn’t lose any of those features, and muscles, nerves, and a gut evolved only once.

The new article in Nature Communications supports the “sponges first” scenario. Click on the screenshot below to read the article, see the pdf here, and find the reference at the bottom of this post. The authors used a new way of making phylogenies using DNA data, dubbed “partition site-heterogeneous models” to eliminate artifacts that may have erroneously shown ctenophores as the sister group of other animals. I’m not going to explain that method and, to be sure, I don’t understand it. In fact, the main results of the paper for the layperson can be described very simply: the new method shows that sponges are the sister group to all animals, a result that makes sense.

I just gave you the punch line, but have to add that the controversy isn’t settled. It is settling, however, as more and more biologists come around to the “sponges split off first” scenario. (I won’t even mention the controversy about the placozoans and ctenophores, and where they fit with relationship to Cnidaria.) Let me just put in the authors’ paragraph where they say that their finding of sponges as the sister group of all other animals is definitive: (my emphasis):

Several studies have already shown that gene family and unpartitioned phylogenomic analyses using more sophisticated substitution models reject Ctenophora sister in favour of Porifera sister. Here, we have consolidated these findings by directly showing that the primary remaining lines of evidence supporting Ctenophora sister, partitioned phylogenomics and measures of underlying support (such as ΔPSlnl values), do not do so when better-fitting site-heterogeneous models are incorporated into the analysis. Thus, the Ctenophora-sister hypothesis can now be wholly rejected in favour of the traditional Porifera-sister scenario of animal evolution, wherein the animal ancestor did not possess key traits such as a nervous system, muscles or a mouth and gut.

Ctenophores as the sister group is now “wholly rejected”! I suspect that not all animal systematists would accept this hypothesis. I do, tentatively, but I don’t fully understand the complex methods of analyzing DNA data (they used 60 animal groups, 406 genes, and 88,384 DNA sites).  My view of these complex methods is the same one that my academic grandfather, Theodosius Dobzhansky, held towards the experts in mathematical population genetics (Dobzhansky was innumerate): “Papa knows best.”

For a fuller explication of the conflict, as well as an overview of animal evolution in general, you can’t do better than Matthew’s 2018 Discovery PROGRAM on the BBC. The controversy about sponges-first versus ctenophores-first starts at 17:45. This program is very good, involves interviews with a lot of different biologists, and should be very clear to the sentient layperson. Plus it’s only half an hour long. Spend this Sunday learning a bit about animal evolution!

Click on the screenshot to hear the show:

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Redmond, A.K., and A. McLysaght 2021. Evidence for sponges as sister to all other animals from partitioned phylogenomics with mixture models and recoding. Nat Commun 12, 1783 (2021). https://doi.org/10.1038/s41467-021-22074-7

Nobel Prize for Physiology or Medicine goes to three for discovering the Hepatitis C virus

October 5, 2020 • 7:00 am

Knowing that the first Nobel Prize for science would be awarded today—in Physiology or Medicine—I made a contest in which readers were to guess just one winner of each of the three science prizes plus the winner of this year’s Literature Nobel.

Well, the first prize was awarded this morning, and the contest is already over. Everyone lost (see here and here).

Granted, this was not an easy one to guess. The award in fact went to three people—Harvey Alter, Michael Houghton, and Charles Rice—with each getting a third of the prize money. The award was given for the discovery of the virus that causes Hepatitis C.  Here’s part of the press release from the Nobel Prize site:

This year’s Nobel Prize is awarded to three scientists who have made a decisive contribution to the fight against blood-borne hepatitis, a major global health problem that causes cirrhosis and liver cancer in people around the world.

Harvey J. Alter, Michael Houghton and Charles M. Rice made seminal discoveries that led to the identification of a novel virus, Hepatitis C virus. Prior to their work, the discovery of the Hepatitis A and B viruses had been critical steps forward, but the majority of blood-borne hepatitis cases remained unexplained. The discovery of Hepatitis C virus revealed the cause of the remaining cases of chronic hepatitis and made possible blood tests and new medicines that have saved millions of lives.

. . . The Nobel Laureates’ discovery of Hepatitis C virus is a landmark achievement in the ongoing battle against viral diseases (Figure 2). Thanks to their discovery, highly sensitive blood tests for the virus are now available and these have essentially eliminated post-transfusion hepatitis in many parts of the world, greatly improving global health. Their discovery also allowed the rapid development of antiviral drugs directed at hepatitis C. For the first time in history, the disease can now be cured, raising hopes of eradicating Hepatitis C virus from the world population. To achieve this goal, international efforts facilitating blood testing and making antiviral drugs available across the globe will be required

Here’s the video of the award with details about the winners, and giving some scientific background; the action starts at 12:50. It’s worth listening to the 20 minutes of science, as you’ll learn a lot. There’s also an interview with the Secretary of the Prize Committee beginning at 34:34.

I guess the prize for CRISPR-Cas9 will have to wait for another year.

Matthew’s theory, which is his, about why Covid-19 and other viral infections often reduce one’s sense of smell

April 1, 2020 • 11:52 am

Matthew tweeted his new theory, which is his, about why Covid-19 patients very often experience “smell blindness”, technically known as anosmia—the loss of one’s sense of smell (which of course also reduces one’s ability to taste). I asked him if he wanted to post it here, and he’s rewritten it so it’s understandable by the science-friendly layperson. And so, without further ado:

A hypothesis to explain why the Covid-19 virus affects the sense of smell in some people

By Matthew Cobb

 

In a recent study by King’s College, London of 579 people who reported having a positive Covid-19 test, 59% said they had reported a loss of smell or taste. This is not unique to Covid-19 – many other viruses can cause the same effect. It has never been quite clear how this occurs. The great amount of attention being paid to Covid-19 has helped reveal one possible mechanism.

We smell volatile molecules, but we don’t directly detect them in the air – our smell neurons would shrivel up and die. Our neurons are protected by a layer of mucus, and the smell molecules have to get through that.

The chemical structure of most smells means they are what is known as hydrophobic – they won’t dissolve easily in water, such as that found in the mucus. It is widely thought that the smells are transported by rather mysterious chaperones called olfactory binding proteins (OBPs).

These molecules are secreted into the mucus by cells called Bowman’s cells in the olfactory epithelium – the layer of skin, high up in the roof of your nasal cavity, which is where you smell things. Many scientists think that OBPs deliver the odour to the receptor on the neuron, and then appear to be taken up by cells called sustentacular cells which lie next door.

A paper that appeared a few days ago suggests that our olfactory neurons don’t express the ACE proteins that are the virus target, and that disruption to our neurons is therefore not the cause of anosmia. However, other cells in the olfactory epithelium, the sustentacular cells and the Bowman’s cells that produce OBPs, do express the ACE protein. Both these cell types are involved in the way that OBPs work.

If the virus is attacking these cells, then the metabolism of OBPs, and thereby the balance of detection of molecules will be altered. This may explain the widespread reports of anosmia following covid-19 infection, and, in some cases like that of the science journalist Adam Rutherford, who had symptoms of covid-19,  hyperosmia (increased sensitivity). Sustentacular cells are also electrically active in newborn mice, perhaps indicating a more complex function for these cell types.

All this suggests that the return of normal olfactory functioning in patients with covid-19, or other coronaviruses, which may also cause these effects, probably depends on the time it takes for the Bowman’s cells and the sustentacular cells to recover.

A simpler explanation – advanced by @stevenmunger on Twitter in response to this – is that infection of these specific cell types merely causes inflammation, which alters tissue function. There may be other hypotheses, too. And some scientists don’t agree that OBPs play much of a role at all in olfaction. “For example, although humans have a number of genes that encode for OBPs, only one kind has so far been identified in the human olfactory epithelium. We clearly need to understand more about this aspect of how we smell.”

Whatever the exact mechanism involved, as Prof Tim Spector of King’s College said: “When combined with other symptoms, people with loss of smell and taste appear to be three times more likely to have contracted Covid-19 according to our data, and should therefore self-isolate for seven days to reduce the spread of the disease.”

For advice on living with anosmia:

fifthsense.org.uk

abscent.org.uk

BBC report of the King’s College study:

https://www.bbc.co.uk/news/health-52111606

References:

Brann et al (2020) – Gene expression in olfactory epithelium, on covid-19 and entry:

Strotmann & Breer (2011) – OBPs and sustentacular cells

Vogalis et al (2005) – Electrical activity in sustentacular cells

Badonnel et al (2009) – OBPs secreted by Bowman’s cells

 

A prediction: Do blind people dream?

December 24, 2018 • 6:30 pm

 

CLARIFICATION; By “dreaming” here, I was asking whether blind people have visual dreams.

The NBC News tonight broadcast a segment about a little girl who was born blind but has a really positive attitude: she has her own upbeat show on local radio, reading from a Braille script, and says that the only thing she can’t do is “see.”

That instantly got me wondering: Do blind people dream?  And here’s a prediction—actually three predictions—before I’ve checked on the Internet. (I don’t think I’ll check until tomorrow, or I’ll wait until a reader tells me.)

The first prediction, which is mine, is based on the supposition that if someone is born blind, they’ve never been able to process visual input and therefore couldn’t experience it in their brain. Therefore, I predict that they would not be able to dream.

But people who go blind after they’re born would have developed the brain ability and experience of seeing and would have the neural ability to dream. BUT—the third prediction—the longer they’ve been blind, the less reinforcement of their brain-eye connection they’d have, and I predict that they’d gradually lose the ability to dream, or at least the frequency of dreaming would wane.

It’s strange that I’ve never thought about this before.